Mercury is a global pollutant and potent neurotoxin. Methylmercury is one of the most toxic forms of mercury due to its ability to cross the blood brain and placental barriers. Fish consumption is considered the primary exposure methylmercury pathway because this form of mercury is efficiently biomagnified in the aquatic food web and the mercury dose from seafood is greater than 95% methylmercury in predatory fish, like tuna and shark. Historical methylmercury poisonings in Japan and Iraq confirmed human health impacts from methylmercury exposure were most severe in the developing fetus due to irreversible neural damage. The current paradigm, with respect to maternal ingestion of fish during gestation, supports consumption of fish high in omega-3 fatty acids but low in methylmercury to gain the benefits of fish ingestion (i.e., promote prenatal neurodevelopment), while minimizing exposure of the fetus to methylmercury. However, there remains a critical knowledge gap concerning the effect of low-level maternal methylmercury exposure on the developing fetus in the absence of (or lower level of) omega-3 fatty acids. The primary aim of this study is to address this knowledge gap. In the town of Wanshan, Guizhou province, southwestern China, a legacy of mercury contamination from 600 years of mercury mining has severely polluted the air, soil and water. In this region, rice ingestion was reported as the primary methylmercury exposure pathway, not fish. The proposed study includes recruitment of a mother-offspring cohort in Wanshan, China, to investigate offspring neurodevelopment among a population where rice is a staple food and mercury contamination is elevated. All previous studies concerning maternal methylmercury exposure and offspring health included populations where fish ingestion was the primary exposure pathway. This study will examine methylmercury exposure in the absence of the same beneficial micronutrients associated with fish ingestion. The specific aim is to establish for the first time, whether a relationship exists between prenatal methylmercury exposure and offspring neurodevelopment in a population where rice is the primary maternal methylmercury exposure pathway, while accounting for other known confounders of concern, including maternal nutritional status and other indirect measures. Results from this study will enable health professionals to develop more protective guidelines to reduce irreversible neurodevelopmental damage to offspring due to prenatal methylmercury exposure. Additionally, rice is a staple food for more than half the world's population; therefore, it is critical to investigate the potential health risks of methylmercury exposure through maternal ingestion of rice to the developing fetus, the most susceptible population to the deleterious effects of methylmercury.